Some known implantable medical devices (IMD) for cardiac applications, such as pacemakers, are used to deliver pacing pulses to a cardiac chamber to induce a depolarization of that chamber, which is followed by mechanical contraction of that chamber, when a patient's own intrinsic rhythm fails. The IMD further includes sensing circuits that sense electrical activity for the detection of intrinsic cardiac events such as intrinsic atrial depolarizations (detectable as P waves) and intrinsic ventricular depolarizations (detectable as R waves). By monitoring electrical activity, the IMD is able to determine the intrinsic rhythm of the heart and provide stimulation pacing pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle to help stabilize the electrical rhythm of the heart.
Some known IMDs utilize one or more electrically-conductive leads that extend from a remotely-located canister or pulse-generator and traverse blood vessels and cardiac chambers to affix connected electrodes to the heart. The housing or canister, referred to as a “can”, has electronics and a power source. The can, including the power and processing circuitry, and a portion of the leads are located outside of the patient's heart, and the power and data signals are relayed to and from the heart via the leads.
Since the leads traverse the vascular system and connect to the heart from the remote can, infectious organisms, most commonly bacteria, may be introduced into the patient's systemic circulation and heart through the leads, thereby increasing the risk of infection within the heart. Additionally, because the IMD is located outside of the heart, most often in a pre-pectoral pocket, the patient may be susceptible to Twiddler's syndrome. Twiddler's syndrome is typically characterized by a subconscious, inadvertent, or infrequently deliberate rotation of the IMD within a subcutaneous pocket created in the patient into which the IMD is implanted. This results in lead retraction and wrapping around the IMD and as a result, leads may dislodge from the endocardium. Further consequences include stimulation of the diaphragm, phrenic nerve, pectoral muscles, or brachial plexus as a result of the displaced lead. In addition to the foregoing complications, the presence of leads may be associated with and/or cause a number of additional complications.
To mitigate the limitations and complications associated with transvenous leads and the associated IMD, smaller sized devices configured for intra-cardiac implant without the need for transvenous leads have been proposed. These devices, termed “leadless pacemakers”, are devoid of leads that pass out of the heart to another component, such as a can located outside of the heart. The entire device is configured to be attached to the heart. Thus, the power source and the processing circuitry are contained within the device that is attached to the heart. The leadless pacemakers include electrodes that are affixed directly to the can of the device, instead of being separated by a distance traversed by one or more leads. Each leadless pacemaker is capable of local pacing and sensing in the chamber of the heart where it is implanted.
The leadless pacemakers that have been proposed thus far offer limited functional capability. For example, when the power source (e.g., battery) is depleted and/or the processing circuitry needs to be updated, the entire device must be removed from the heart. Removing the pacemaker device from the myocardial tissue of the heart may be difficult and may damage the surrounding cardiac and/or vascular tissue. In some cases, the removal may even tear the myocardial tissue. Removing the leadless pacemaker from a fixated position may be complicated by fibrosis around the fixation mechanism, which occurs when tissue grows around and at least partially envelops the fixation system of the leadless pacemaker after attaching the pacemaker to the tissue wall.
Once the depleted leadless pacemaker is removed, additional problems may be encountered when implanting a new replacement leadless pacemaker. For example, when implanting the replacement pacemaker, a preferred location to affix the device is in the same location as the previous pacemaker due to stable sensing and pacing values and knowledge that the location is stable to accommodate the implanted device. However, identifying the previous location may be very difficult and the presence of fibrosis at the site of previous fixation may limit accessibility to this exact location. In addition, implanting a new device in the same location as the device that was extracted may be difficult due to tissue damage caused by the extraction. The removal process may render the underlying tissue and substrate less stable, less efficient for pacing, and more prone for perforation during the implantation of the replacement pacemaker. Locating the replacement pacemaker at a different location than the previous pacemaker may change the pacing and sensing thresholds, requiring additional steps to calibrate the sensing circuitry and adjust the pacing circuitry, while still risking reduced performance due to a sub-optimal and less stable implant location. Accordingly, it is important to avoid detaching the leadless pacemaker electrode from the tissue wall on which it is mounted, which would disturb the surrounding tissue as well as the pacing and sensing thresholds.